scholarly journals Regional Changes in Myocardial Strain Predict Ventricular Remodelling after Myocardial Infarction in a Large Animal Model

2021 ◽  
Author(s):  
Doyin S. Mansell ◽  
Vito D. Bruno ◽  
Eva Sammut ◽  
Amedeo Chiribiri ◽  
Tom Johnson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Circumferential Strain ◽  
Myocardial Strain ◽  
Left Ventricular ◽  
Large Animal Model ◽  
Large Animal ◽  
Strain Rates ◽  
Ventricular Remodelling ◽  
Early Predictors ◽  
Over Time

Abstract To identify early predictors of late left ventricular remodelling (LVR) post-myocardial infarction (MI) and related molecular signatures, a porcine model of closed-chest balloon MI was used. LVR was assessed by cardiac magnetic resonance imaging (CMRI) at baseline, 12–48 hours (acute), and 5–6 weeks (chronic) post-MI. Changes in myocardial strain and strain rates were derived from CMRI data. Tissue proteomics was compared between infarcted and non-infarcted territories. Peak values of left ventricular (LV) apical circumferential strain (ACS) changed over time together with peak global circumferential strain (GCS) while peak GLS epicardial strains or strain rates did not change over time. LVR post-MI enhanced abundance of 39 proteins in infarcted LV territories,21 of which correlated with LV equatorial circumferential strain rate (ECSR). The strongest associations were observed for D-3-phosphoglycerate dehydrogenase (D-3PGDH), cysteine and glycine-rich protein-2 (CG-RP-2), and secreted frizzled-related protein 1 (sFRP1). Results indicate that early changes in regional peak ACS predict late LV remodelling and LVR post-MI is associated with augmented levels of D-3PGDH and sFRP1, which show the strongest association with peak ECSR. These findings might help to prevent LVR post-MI by influencing/directing LV unloading strategies or by pharmacological control of tissue levels of D-3PGDH and sFRP1.

scholarly journals Acute regional changes in myocardial strain may predict ventricular remodelling after myocardial infarction in a large animal model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
D. S. Mansell ◽  
V. D. Bruno ◽  
E. Sammut ◽  
A. Chiribiri ◽  
T. Johnson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Circumferential Strain ◽  
Myocardial Strain ◽  
Left Ventricular ◽  
Large Animal Model ◽  
Large Animal ◽  
Strain Rates ◽  
Ventricular Remodelling ◽  
Tissue Levels ◽  
Over Time

AbstractTo identify predictors of left ventricular remodelling (LVR) post-myocardial infarction (MI) and related molecular signatures, a porcine model of closed-chest balloon MI was used along with serial cardiac magnetic resonance imaging (CMRI) up to 5–6 weeks post-MI. Changes in myocardial strain and strain rates were derived from CMRI data. Tissue proteomics was compared between infarcted and non-infarcted territories. Peak values of left ventricular (LV) apical circumferential strain (ACS) changed over time together with peak global circumferential strain (GCS) while peak GLS epicardial strains or strain rates did not change over time. Early LVR post-MI enhanced abundance of 39 proteins in infarcted LV territories, 21 of which correlated with LV equatorial circumferential strain rate. The strongest associations were observed for D-3-phosphoglycerate dehydrogenase (D-3PGDH), cysteine and glycine-rich protein-2, and secreted frizzled-related protein 1 (sFRP1). This study shows that early changes in regional peak ACS persist at 5–6 weeks post-MI, when early LVR is observed along with increased tissue levels of D-3PGDH and sFRP1. More studies are needed to ascertain if the observed increase in tissue levels of D-3PGDH and sFRP1 might be casually involved in the pathogenesis of adverse LV remodelling.

scholarly journals Delivery of a matrix metalloproteinase-responsive hydrogel releasing TIMP-3 after myocardial infarction: effects on left ventricular remodeling

2018 ◽  
Vol 315 (4) ◽  
pp. H814-H825 ◽  
Author(s):  
Brendan P. Purcell ◽  
Shayne C. Barlow ◽  
Paige E. Perreault ◽  
Lisa Freeburg ◽  
Heather Doviak ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinases ◽  
Ventricular Remodeling ◽  
Left Ventricular ◽  
Large Animal Model ◽  
Left Ventricular Geometry ◽  
Relative Reduction ◽  
Large Animal ◽  
Early Reperfusion ◽  
Localized Delivery

Although improvements in timing and approach for early reperfusion with acute coronary syndromes have occurred, myocardial injury culminating in a myocardial infarction (MI) remains a common event. Although a multifactorial process, an imbalance between the induction of proteolytic pathways, such as matrix metalloproteinases (MMPs) and endogenous tissue inhibitors of metalloproteinase (TIMPs), has been shown to contribute to this process. In the present study, a full-length TIMP-3 recombinant protein (rTIMP-3) was encapsulated in a specifically formulated hyaluronic acid (HA)-based hydrogel that contained MMP-cleavable peptide cross-links, which influenced the rate of rTIMP-3 release from the HA gel. The effects of localized delivery of this MMP-sensitive HA gel (HAMMPS) alone and containing rTIMP-3 (HAMMPS/rTIMP-3) were examined in terms of the natural history of post-MI remodeling. Pigs were randomized to one of the following three different groups: MI and saline injection (MI/saline group, 100-μl injection at nine injection sites, n = 7), MI and HAMMPS injection (MI/HAMMPS group; 100-μl injection at nine injection sites, n = 7), and MI and HAMMPS/rTIMP-3 injection (MI/HAMMPS/rTIMP-3 group; 20-μg/100-μl injection at nine injection sites, n = 7). Left ventricular (LV) echocardiography was serially performed up to 28 days post-MI. LV dilation, as measured by end-diastolic volume, and the degree of MI wall thinning were reduced by ~50% in the HAMMPS/rTIMP-3 group ( P < 0.05). Furthermore, indexes of heart failure progression post-MI, such as LV filling pressures and left atrial size, were also attenuated to the greatest degree in the HAMMPS/rTIMP-3 group. At 28 days post-MI, HAMMPS/rTIMP-3 caused a relative reduction in the transcriptional profile for myofibroblasts as well as profibrotic pathways, which was confirmed by subsequent histochemistry. In conclusion, these findings suggest that localized delivery of a MMP-sensitive biomaterial that releases a recombinant TIMP holds promise as a means to interrupt adverse post-MI remodeling. NEW & NOTEWORTHY The present study targeted a myocardial matrix proteolytic system, matrix metalloproteinases (MMPs), through the use of a recombinant tissue inhibitor of MMPs incorporated into a MMP-sensitive hydrogel, which was regionally injected using a large animal model of myocardial infarction. Left ventricular geometry and function and indexes of myocardial remodeling were improved with this approach and support the advancement of localized therapeutic strategies that specifically target the myocardial matrix.

scholarly journals Early Predictors of Heart Failure Progression in Patients After Myocardial Infarction

Kardiologiia ◽  
2020 ◽  
Vol 60 (11) ◽  
pp. 84-93
Author(s):  
V. E. Oleynikov ◽  
E. V. Dushina ◽  
A. V. Golubeva ◽  
Ju. A. Barmenkova
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Global Longitudinal Strain ◽  
Myocardial Strain ◽  
Radial Strain ◽  
Heart Rhythm ◽  
Left Ventricular ◽  
Heart Rhythm Variability ◽  
St Segment Elevation ◽  
Early Predictors

Aim      To identify early predictors for progression of chronic heart failure (CHF) in patients with ST-segment elevation myocardial infarction (STEMI).Material and methods  The study included 113 patients with STEMI aged 52 (95 % confidence interval, 36 to 65) years. 24-h ECG monitoring was performed with assessment of ventricular late potentials, QT dispersion, heart rhythm turbulence (HRT), and heart rhythm variability (HRV); XStrain 2D echocardiograpy with determination of volumetric parameters, myocardial strain characteristics and velocities; and measurement of brain natriuretic peptide (BNP) concentrations. The endpoint was CHF progression during 48 weeks of follow-up, which was observed in 26 (23 %) patients. Based on the outcome, two groups were isolated, with CHF progression (Prg) (26(23%)) and with a relatively stable CHF postinfarction course (Stb) (87 (77 %)).Results At 12 weeks following MI, the Prg group showed increases in left ventricular (LV) end-diastolic dimension (EDD) (р<0.05) and end-diastolic and end-systolic volumes (EDV, ESV), (р<0.01), and EDV and ESV indexes (EDVi and ESVi, р<0.01). In this group, global longitudinal strain (GLS) was decreased at 24 weeks (р<0.05) and global radial strain (GRS) was decreased at 48 weeks (р=0.0003). In the Prg group, values of strain parameters (GLS, global circular strain (GCS), and GRS) were lower at all times. At 7-9 days, 24 weeks, and 48 weeks, the proportion of patients with pathological HRT was higher in the Prg group (38, 27, and 19 % for the Prg group vs 14 % (р=0.006); 3,4 % (р=0.001), and 2.3 % (р=0.002) for the Stb group, respectively). Only in the Stb group, increases in HRV were observed (SDNNi by 13 % (р=0.001), rMSSD by 24 % (р=0.0002), TotP by 49 % (р=0.00002), VLfP by 23 % (р=0.003), LfP by 22 % (р=0.008), and HfP by 77 % (р=0.002). At 7-9 days of MI, the Stb group had greater values of SDANN (р=0.013) and HfP (р=0.01). CHF progression correlated with abnormal values of turbulence onset (TO), disturbed HRT, increased BNP levels and LV ESD, and low values of GLS, GCS, and GRS. Combined assessment of HRT, LV ESD, and GLS at 7–9 days after STEMI allows identifying patients with high risk for CHF progression in the next 48 weeks.Conclusion      The markers for CHF progression after STEMI include abnormal TO values, disturbed HRT, increased BNP levels and LV ESD, and low values of GLS, GCS, and GRS. The multifactor logistic regression analysis revealed early predictors of CHF in the postinfarction period, including abnormal TO, increased LV ESD, and reduced GLS.  

Bioengineering Quantification of Left Ventricular Remodeling Following Myocardial Infarction

2009 ◽  
Author(s):  
Changfu Wu ◽  
Won-Bae Chang ◽  
Marc Gibber ◽  
P. Griffith Bartley ◽  
Zhongjun J. Wu
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Remodeling ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Large Animal Model ◽  
Western World ◽  
Large Animal ◽  
Lv Remodeling ◽  
Geometric Changes

Myocardial infarction (MI)-induced heart failure is the prevailing cause of morbidity and mortality in the western world. It is the sequela of the deleterious left ventricular (LV) remodeling process. So far, the mechanisms of the cardiac remodeling process are not completely understood. A clinically relevant large animal model is an essential vehicle for studying the mechanisms of cardiac remodeling. In our laboratory, we have developed a reproducible ovine model of post-infarct chronic cardiac remodeling. Throughout the study period of an animal, the functional and geometric changes of the LV were monitored by echocardiographic and bioengineering means.

scholarly journals A novel method of standardized myocardial infarction in aged rabbits

2017 ◽  
Vol 312 (5) ◽  
pp. H959-H967 ◽  
Author(s):  
Patrick J. Morrissey ◽  
Kevin R. Murphy ◽  
Jean M. Daley ◽  
Lorraine Schofield ◽  
Nilufer N. Turan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Minimally Invasive ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Large Animal Model ◽  
Large Animal ◽  
Free Wall ◽  
Left Ventricular Free Wall ◽  
Invasive Approach ◽  
Age Cohorts

The incidence of both myocardial infarction (MI) and sudden cardiac death increases with age. Here, we describe the development of a minimally invasive large animal model of MI that can be applied to young or aged animals. We demonstrate that rabbit coronary anatomy is highly variable, more so than described in previous literature. In this work, we categorize the coronary pattern of 37 young rabbits and 64 aged rabbits. Aged rabbits had a higher degree of branching from the left main coronary artery. Standardizing the model across age cohorts required a new approach, targeting an area of myocardium rather than a specific vessel. Here, we present a method for achieving a reproducible infarct size, one that yielded a consistent scar encompassing ~30% of the apical left ventricular free wall. The model’s consistency allowed for more valid comparisons of MI sequelae between age cohorts. NEW & NOTEWORTHY This study describes the coronary angiographic imaging of young and aged rabbits. We developed and improved a novel minimally invasive approach for coil embolization that targets a specific area of myocardium and yielded a consistent scar encompassing ~30% of the left ventricular free wall of young and aged rabbit hearts.

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